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    Bernal P, Civantos C, Filloux A, Llamas MAet al.,

    Type VI secretion in the plant growth promoting rhizobacteria Pseudomonas putida

    , FEMS Microbiology Congress 2015

    BackgroundBacterial type VI secretion systems (T6SSs) are recently discovered nanomachines used to inject effectors into prokaryotic or eukaryotic cells. Therefore, T6SSs are involved in both inter-bacterial competition and bacterial pathogenesis.ObjectivesThe aim is the study of the T6SS of Pseudomonas putida a soil bacterium with the capacity to colonise the root of crop plants. The colonisation by this bacterium provides growth advantages to the plant and, importantly, protection against plant pathogens. This makes P. putida a relevant biocontrol agent. Since T6SS is mainly used by environmental bacteria for interbacterial competition, one might speculate that T6SSs play a relevant role in the biocontrol properties of P. putida. Methods• in silico analysis of P. putida KT2440 genome • Competition assays to determine H1-T6SS activity and for the identification of H1-T6SS targets.• Regulatory studies: qRT-PCR, transcriptional fusionsConclusionsThe in silico analysis has revealed the existence of three putative T6SSs (H1, H2, and H3). The clusters contain the genes encoding the conserved core components and some accessories, including regulatory proteins and toxins-immunity pairs. Additional T6SS-related genes are found scattered on the chromosome.By competition assays we have determined that H1-T6SS is active and that mutants in H1-T6SS structural components lack the ability to kill model prey strains. Moreover, the system can be used to kill serious phytopathogens such as Pseudomonas syringae in in vitro assays. Interestingly, the H1-T6SS is induced in stationary phase and controlled by the global regulators RetS and GacS-GacA, and by two alternative sigma factors, RpoS and RpoN.

    Dominguez-Huttinger E, Boon NJ, Clarke TB, Tanaka RJet al.,

    Mathematical modelling of colonization, invasive infection and treatment of Streptococcus pneumoniae

    , Frontiers in Physiology, ISSN: 1664-042X

    Streptococcus pneumoniae (Sp) is a commensal bacterium that normally resides on the upper airway epithelium without causing infection. However, factors such as co-infection with influenzavirus can impair the complex Sp-host interactions and the subsequent development of manylife-threatening infectious and inflammatory diseases, including pneumonia, meningitis or evensepsis. With the increased threat of Sp infection due to emergence of new antibiotic resistant Sp strains, there is an urgent need for better treatment strategies that effectively prevent progression of disease triggered by Sp infection, minimizing the use of antibiotics. The complexity of the host-pathogen interactions has left the full understanding of underlying mechanisms of Sp-triggered pathogenesis as a challenge, despite its critical importance in the identification of effective treatments. To achieve a systems-level and quantitative understandingof the complex and dynamically-changing host-Sp interactions, here we developed a mechanisticmathematical model describing dynamic interplays between Sp, immune cells, and epithelial tissues, where the host-pathogen interactions initiate. The model serves as a mathematical framework that coherently explains various in vitro and in vivo studies, to which the model parameters were fitted. Our model simulations reproduced the robust homeostatic Sp-host interaction, as well asthree qualitatively different pathogenic behaviours: immunological scarring, invasive infectionand their combination. Parameter sensitivity and bifurcation analyses of the model identified the processes that are responsible for qualitative transitions from healthy to such pathologicalbehaviours. Our model also predicted that the onset of invasive infection occurs within less than 2 days from transient Sp challenges. This prediction provides arguments in favour of the use of vaccinations, since adaptive immune responses cannot be developed de novo in such a short time. We further designe

    Mostowy S,

    Chytrid fungus infection in zebrafish demonstrates that the pathogen can parasitise non-amphibian vertebrate hosts

    , Nature Communications
    Pallett MA, Crepin VF, Serafini N, Habibzay M, Kotik O, Sanchez-Garrido J, Di Santo J, Shenoy AR, Berger CN, Frankel GMet al.,

    Bacterial Virulence Factor Inhibits Caspase-4/11 Activation in IntestinalEpithelial Cells

    , Mucosal Immunology, ISSN: 1935-3456

    The human pathogen enteropathogenic Escherichia coli (EPEC), as well as the mouse pathogen Citrobacter rodentium, colonize the gut mucosa via attaching and effacing lesion formation and cause diarrheal diseases. EPEC and C. rodentium type III secretion system (T3SS) effectors repress innate immune responses and infiltration of immune cells. Inflammatory caspases such as caspase'1 and caspase'4/11 are crucial mediators of host defense and inflammation in the gut via their ability to process cytokines such as IL'1β and IL'18. Here we report that the effector NleF binds the catalytic domain of caspase'4 and inhibits its proteolytic activity. Following infection of intestinal epithelial cells (IECs) EPEC inhibited caspase'4 and IL'18 processing in an NleF'dependent manner. Depletion of caspase'4 in IECs prevented the secretion of mature IL'18 in response to infection with EPEC@nleF. NleF'dependent inhibition of caspase'11 in colons of mice prevented IL'18 secretion and neutrophil influx at early stages of C. rodentium infection. Neither wild'type C. rodentium nor C. rodentium@nleF triggered neutrophil infiltration or IL'18 secretion in Cas11 or Casp1/11 deficient mice. Thus, IECs play a key role in modulating early innate immune responses in the gut via a caspase'4/11 ' IL'18 axis, which is targeted by virulence factors encoded by enteric pathogens

    Wilkinson RJ, Esmail H, Lesosky M, Lai RP, Wilkinson KA, Graham CM, Coussens AK, Oni T, Warwick J, Said-Hartley Q, Koegenelburg CF, Walzl G, Flynn JL, young DB, Barry CE, O'Garra Aet al.,

    [18F]-FDG PET/CT characterisation of progressive HIV-associated tuberculosis

    , Nature Medicine, ISSN: 1546-170X

    Tuberculosis is classically divided into states of latent infection and active disease. Usingcombined positron emission and computed tomography in 35 asymptomatic, antiretroviraltherapy naïve, HIV-1 infected adults with latent tuberculosis, we identified ten individualswith pulmonary abnormalities suggestive of subclinical, active disease who weresignificantly more likely to progress to clinical disease. Our findings challenge theconventional two-state paradigm and may aid future identification of biomarkers predictiveof progression.

    Ale A, Crepin VF, Collins JW, Constantinou N, Habibzay M, Babtie AC, Frankel G, Stumpf MPHet al., 2017,

    Model of Host-Pathogen Interaction Dynamics Links In Vivo Optical Imaging and Immune Responses

    , INFECTION AND IMMUNITY, Vol: 85, ISSN: 0019-9567
    Bernal P, Allsopp LP, Filloux A, Llamas MAet al., 2017,

    The Pseudomonas putida T6SS is a plant warden against phytopathogens

    , ISME JOURNAL, Vol: 11, Pages: 972-987, ISSN: 1751-7362
    Bosi E, Fondi M, Orlandini V, Perrin E, Maida I, de Pascale D, Tutino ML, Parrilli E, Lo Giudice A, Filloux A, Fani Ret al., 2017,

    The pangenome of (Antarctic) Pseudoalteromonas bacteria: evolutionary and functional insights

    , BMC GENOMICS, Vol: 18, ISSN: 1471-2164
    Brown RL, Clarke TB, 2017,

    The regulation of host defences to infection by the microbiota

    , IMMUNOLOGY, Vol: 150, Pages: 1-6, ISSN: 0019-2805
    Dominguez-Huettinger E, Boon NJ, Clarke TB, Tanaka RJet al., 2017,

    Mathematical Modeling of Streptococcus pneumoniae Colonization, Invasive Infection and Treatment

    , FRONTIERS IN PHYSIOLOGY, Vol: 8, ISSN: 1664-042X

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